Aging and the mitochondrial response to exercise training, measured by noninvasive 31P magnetic resonance spectroscopy

通过无创 31P 磁共振波谱测量衰老和线粒体对运动训练的反应

基本信息

批准号：
10417265
负责人：
OWEN T. CARMICHAEL
金额：
$ 61.05万
依托单位：
LSU PENNINGTON BIOMEDICAL RESEARCH CTR
依托单位国家：
美国
项目类别：
财政年份：
2020
资助国家：
美国
起止时间：
2020-09-01 至 2024-05-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10417265
关键词：
Acute Address Adult Aerobic Aerobic Exercise Age Aging Ancillary Study Attenuated Automobile Driving Bioenergetics Bioinformatics Biologic Characteristic Biological Biology Collaborations Collection DNA Methylation Data Disease Elderly Event Exercise Funding Health Health Benefit Individual Knowledge Light Link Magnetic Resonance Spectroscopy Measurement Measures Mitochondria Modality Molecular Molecular Profiling Multiomic Data Muscle Muscle Mitochondria Non-Insulin-Dependent Diabetes Mellitus Outcome Pathway interactions Persons Phenotype Phosphocreatine Physical Fitness Physical Function Physical activity Physiological Prevention Principal Investigator Proteomics Publishing Recovery Regulation Reporting Resistance Role Skeletal Muscle Technology Time Training Transducers United States National Institutes of Health VO2max Variant Work age group age related base cardiometabolism cardiorespiratory fitness clinically relevant epigenomics exercise prescription exercise training experience healthy aging improved in vivo inter-individual variation lipidomics member middle age mode of exercise muscular structure novel precision medicine programs resistance exercise response strength training transcriptomics vastus lateralis virtual young adult

项目摘要

Program Director/Principal Investigator (Last, First, Middle): Project Summary Reduced skeletal muscle mitochondrial oxidative capacity of skeletal muscle has been implicated in aging- related declines in cardiorespiratory fitness, physical functioning, and cardiometabolic health. Although exercise training in older adults increases mitochondrial capacity, virtually all of the data is reported in terms of average responses within groups. Yet within groups, there is enormous inter-individual variation in these responses. Two specific questions remain regarding the significance and implications of exercise-induced changes in mitochondrial capacity. 1) Does exercise improve mitochondrial capacity similarly in older and younger adults? 2) What are the molecular signatures within skeletal muscle that associate with improvements in mitochondrial capacity in older and younger adults? We will address these major gaps in knowledge by objectively assessing the spectrum of mitochondrial capacity responses to exercise in vivo, investigating the underlying molecular regulation of exercise responses, and relating the mitochondrial responses and molecular factors to clinically-relevant outcomes such as exercise-induced improvements in cardiorespiratory fitness (VO2max). The NIH-funded Molecular Transducers of Physical Activity Consortium (MoTrPAC) funds collection of comprehensive molecular signatures from biospecimens before and after 12 weeks of aerobic and resistance exercise training in healthy adults spanning the adult age span. This ancillary study will synergize with MoTrPAC and will add measurements of mitochondrial capacity of the skeletal muscle via non-invasive 31P magnetic resonance spectroscopy (31P-MRS) before and after training in 420 individuals across a wide age range (18 to 60+). Aim 1 is to assess differences in the mitochondrial capacity response to exercise training across the agespan and between aerobic and resistance training. Aim 2 is to identify molecular transducers of mitochondrial capacity induced by exercise. Primary hypotheses are that a proportion of individuals will not improve mitochondrial capacity following exercise training regardless of modality; age per se will not correlate with mitochondrial capacity responses; that greater improvements in mitochondrial capacity will associate similarly with greater improvements in cardiorespiratory fitness in younger and older adults; and that mitochondrial capacity responses will be greater with aerobic training compared to resistance training but aerobic-resistance differences will be similar across age groups. The impact of the project is that it will leverage the high-throughput `omics' technologies and exercise studies provided by MoTrPAC to shed light on mechanisms underlying the variation in mitochondrial capacity responses linked to health benefits of physical activity in older adults. OMB No. 0925-0001/0002 (Rev. 01/18 Approved Through 03/31/2020) Page Continuation Format Page

计划主任/首席研究员（最后，第一，中间）：项目摘要骨骼肌的骨骼肌线粒体氧化能力降低与衰老有关心肺健康，身体功能和心脏代谢健康的相关下降。虽然老年人的运动训练增加了线粒体的能力，几乎所有数据均以术语报告组中的平均响应。然而，在组中，这些存在很大的个体差异回答。关于锻炼引起的意义和含义仍然存在两个具体问题线粒体能力的变化。 1）在较旧的情况下，运动是否可以提高线粒体能力年轻人？ 2）与改进相关的骨骼肌内分子特征是什么年龄和年轻人的线粒体能力？我们将通过客观地评估线粒体能力对体内运动的反应的频谱，研究了运动反应的基本分子调节，并将线粒体反应和分子相关与临床相关的结果的因素，例如运动引起的心肺适应性改善（vo2max）。 NIH资助的体育活动联盟（MOTRPAC）基金的分子传感器在有氧运动之前和之后，从生物测量中收集了综合分子特征跨成人年龄跨度的健康成年人的抵抗运动训练。这项辅助研究将协同作用使用motrpac，将通过非侵入性增加骨骼肌线粒体能力的测量值 31p磁共振光谱（31p-Mrs）在420名个人训练之前和之后范围（18至60+）。目标1是评估线粒体能力响应对运动训练的差异在整个AGESPAN以及有氧和抵抗训练之间。目标2是鉴定分子传感器通过运动引起的线粒体能力。主要的假设是，一定比例的个人不会运动训练后提高线粒体能力，而不论其方式如何；年龄本身不会相关线粒体能力响应；线粒体能力的更大改善将使同样，年轻和老年人的心肺适应性有所改善；那与抵抗训练相比，有氧训练的线粒体能力反应将更大在年龄组之间，有氧抗性差异将相似。该项目的影响是它将利用Motrpac提供的高通量“ Omics”技术和运动研究线粒体能力响应差异与身体益处有关的机制老年人的活动。 OMB No. 0925-0001/0002（修订版01/18通过03/31/2020批准）页面延续格式页面